NIH R01 · 2024
Endothelial complement C3a receptor mediated cerebral injury in a murine stroke model.
PROJECT SUM MARY: Stroke is the leading cause of adult disability worldwide. Though Intravenous (IV) tissue plasminogen activator (tPA) improves outcome after stroke, it is limited by secondary injury including hemorrhagic transformation, blood-brain-barrier disruption and edema. Activation of complement C3 plays a key role in stroke pathogenesis, as the C3a anaphylatoxin binds to its receptor to exacerbate acute post-ischemic brain injury. However, the mechanisms underlying this injury remain unclear. This study will for the first time define a crucial link between complement C3a receptor associated inflammation and myeloid cell mediated synaptic dysfunction post-stroke. Our long-term goal…
From the public funding record at NIH RePORTER. Describes the funded project, not the reviews below.